Implantable neurostimulation systems have proven therapeutic in a wide variety of diseases and disorders. Pacemakers and Implantable Cardiac Defibrillators (ICDs) have proven highly effective in the treatment of a number of cardiac conditions (e.g., arrhythmias). Spinal Cord Stimulation (SCS) systems have long been accepted as a therapeutic modality for the treatment of chronic pain syndromes, and the application of tissue stimulation has begun to expand to additional applications, such as angina pectoris and incontinence. Deep Brain Stimulation (DBS) has also been applied therapeutically for well over a decade for the treatment of refractory Parkinson's Disease, and DBS has also recently been applied in additional areas, such as essential tremor and epilepsy. Further, in recent investigations, Peripheral Nerve Stimulation (PNS) systems have demonstrated efficacy in the treatment of chronic pain syndromes and incontinence, and a number of additional applications are currently under investigation. Furthermore, Functional Electrical Stimulation (FES) systems such as the Freehand system by NeuroControl (Cleveland, Ohio) have been applied to restore some functionality to paralyzed extremities in spinal cord injury patients.
Each of these implantable neurostimulation systems typically includes one or more electrode carrying stimulation leads, which are implanted at the desired stimulation site, and a neurostimulator implanted remotely from the stimulation site, but coupled either directly to the stimulation lead(s) or indirectly to the stimulation lead(s) via a lead extension. Thus, electrical pulses can be delivered from the neurostimulator to the stimulation electrode(s) to stimulate or activate a volume of tissue in accordance with a set of stimulation parameters and provide the desired efficacious therapy to the patient.
A typical stimulation parameter set may include the electrodes that are sourcing (anodes) or returning (cathodes) the stimulation current at any given time, as well as the amplitude, duration, and rate of the stimulation pulses. The neurostimulation system may further comprise a handheld patient programmer to remotely instruct the neurostimulator to generate electrical stimulation pulses in accordance with selected stimulation parameters. The handheld programmer in the form of a remote control (RC) may, itself, be programmed by a clinician, for example, by using a clinician's programmer (CP), which typically includes a general purpose computer, such as a laptop, with a programming software package installed thereon.
To better understand the effect of stimulation pulses on nerve tissue, reference to FIG. 1 will now be made. As there shown, a typical neuron 1 that can be found in the white matter of the spinal cord or brain includes an axon 2 containing ionic fluid (and primarily potassium and sodium ions) 3, a myelin sheath 4, which is formed of a fatty tissue layer, coating the axon 2, and a series of regularly spaced gaps 5 (referred to as “Nodes of Ranvier”), which are typically about 1 micrometer in length and expose a membrane 6 of the axon 2 to extracellular ionic fluid 7.
When the neuron 1 is stimulated, e.g., via an electrical pulse, an action potential (i.e., a sharp electrochemical response) is induced within the neuron 1. As a result, a transmembrane voltage potential (i.e., a voltage potential that exists across the membrane 6 of the axon 3) changes, thereby conducting a neural impulse along the axon neuron 1 as sodium and potassium ions flow in and out of the axon 3 via the ion channels in the membrane 6. Because ion flow can only occur at the nodes 5 where the membrane 6 of the axon 3 is exposed to the extracellular ionic fluid 3, the neural impulse will actually jump along the axon 3 from one node 6 to the next node 6. In this manner, the myelin sheath 4 serves to speed the neural impulse by insulating the electrical current and making it possible for the impulse to jump from node 6 to node 6 along the axon 3, which is faster and more energetically favorable than continuous conduction along the axon 3. Further details discussing the electro-chemical mechanisms involved with propagating an AP along a neuron are disclosed in U.S. patent Ser. No. 11/752,895, entitled “Short Duration Pre-Pulsing to Reduce Stimulation-Evoked Side-Effects,” which is expressly incorporated herein by reference.
When stimulating target neural tissue, it is sometimes beneficial to block action potentials from being induced in neural tissue not targeted for stimulation in order to avoid adverse side-effects. For example, a high frequency sinusoidal signal can be applied at a location along the spinal cord to block action potentials evoked from a stimulation pulse from being propagated to a non-targeted site, as described in U.S. patent application Ser. No. 12/618,563, entitled “System and Method for Modulating Action Potential Propagation During Spinal Cord Stimulation,” which is expressly incorporated herein by reference. The mechanism of high frequency nerve blocking is the depolarization of the transmembrane voltage potential at a node of Ranvier.
In particular, high frequency blocking is based on the inactivation of sodium channels created by high frequency oscillation of the axonal membrane. With reference to FIG. 2, a computational model shows that a high frequency sinusoidal generator can generate a high frequency sinusoidal signal (waveform A) that can be conveyed to a blocking site of a neuronal axon via a blocking electrode, resulting in a transmembrane voltage potential at the blocking site (waveform F) that oscillates with the applied high frequency sinusoidal signal. Typically, high frequency signals (i.e., signals greater than 2 KHz) evoke an initial action potential that propagates in both directions along the neural axon, as shown during an initial firing period in the transmembrane voltage potential at a node of Ranvier proximal to the blocking site (waveform E) and a transmembrane voltage potential at a node of Ranvier distal to the blocking site (waveform G). However, after the initial firing period, depolarization of the membrane at the blocking site (waveform F) is maintained as long as the high frequency blocking signal is applied. A stimulation pulse train (waveform D) applied to a stimulation site via a stimulation electrode B creates action potentials that propagate to the node of Ranvier proximal to the blocking site (waveform E), but that do not propagate to the node of Ranvier distal to the blocking site (waveform G).
One clinical problem associated with high frequency nerve blocking is that it requires a relatively high amount of power to implement in a clinical setting, since the threshold to block action potentials in a nerve is much higher than the threshold to evoke action potentials in the nerve. Thus, if the amplitude of the intended blocking electrical pulse is not high enough, it would instead stimulate the nerve fibers, potentially causing an adverse stimulation effect. Furthermore, the high frequency blocking signal must be maintained to maintain the blocking effect; otherwise, the nerve fibers will revert back to their normal condition, and will thus, propagate action potentials when stimulated.
Thus, a neurostimulation system and method that is capable of providing high frequency blocking signals in a more power efficient manner is needed.